All metazoans examined to date contain families with repetitive DNA sequences, and suggestions for their function include coordination of the expression of tissue-specific genes, promotion of chromosomal rearrangements such as duplications, inversions, and deletions, a role in speciation, or even no function except self-propagation as "selfish" DNA. We have developed an experimental approach to rapidly characterize and identify rat repeated DNA sequences of potential interest. With this method we made two observations that were unexpected from earlier studies by others on rat repeated DNA: (1) The rat genome contains in addition to the 100,000 member rat satellite I family, at least 5 other highly repeated repeat DNA families. The only high repeat family detected in earlier studies was the rat satellite I family. (2) Most of the members of these highly repeated families (as well as many less highly repeated families) are intermingled in permutated clusters and not interspersed among single copy DNA, which was thought to be the typical organization of most of the repeated DNA in the rat. Detailed examination of the genomic regions harboring two of these highly repeated families is now underway. In parallel studies we examined the structure of the highly transcribed group of low repeat gene families that encode small nuclear RNAs (snRNAs). Initial characterization of cDNa clones that we prepared from the snRNAs synthesized by normal rat kidney cells and by a rat neural tumor line suggests that different snRNA genes may be expressed in different rat cells. We also identified and determined the structure of a new rat satellite DNA family in the rat. Satellite DNA families are of unknown function and generally contain more than 100,000 members which are tandemly arranged in long clusters. These families exhibit a number of curious evolutionary properties. By comparing the structure of our newly discovered satellite DNA with that of the previously discovered one, we learned that homologous interaction among members of the tandem arrays causes the spread of variant family members through tandem arrays. We also learned that some sequence variants are amplified more efficiently than others.